The kidneys are very important organs in the body, used to filter toxins, metabolize, and maintain various body balances. The main manifestation of kidney disease is swelling of the body, especially the eyes, and problems with the urinary system, including hematuria and proteinuria. Among them, renal tubular damage is also a very serious type of kidney damage, which will seriously affect the reabsorption of water by the renal tubules and cause many harms to the body: Renal tubular disorders refer to a group of renal diseases characterized by renal tubular dysfunction. The main clinical manifestations are renal glucosuria, aminoaciduria or low molecular weight proteinuria, electrolyte imbalance and acidosis, with or without abnormal glomerular filtration function. Treatment mainly includes treatment of the primary disease and symptomatic treatment. 1. Causes This group of diseases can be divided into two categories: hereditary and acquired. Hereditary diseases are mostly caused by certain specific gene mutations; acquired diseases are related to infection, poisoning, immunity, endocrine or metabolic abnormalities, etc. 2. Clinical manifestations The main function of the renal tubules is to reabsorb water, electrolytes, glucose, amino acids, proteins, etc. from the tubular filtrate while excreting hydrogen, potassium, uric acid and various metabolites. Impairment of one or more functions of the renal tubules can cause renal tubular disease. ② Impaired renal concentrating function Symptoms include polyuria, diabetes insipidus, thirst, water loss and hypoosmolar urine. ②Renal acidification dysfunction Hyperchloremic metabolic acidosis, dizziness, fatigue, poor appetite, nausea, and alkaline urine may occur. ③Defective tubular reabsorption There may be low potassium, low sodium, low calcium and low magnesium, urine sugar, microalbuminuria, urine β2 microglobulin, α1 microglobulin, N-acetyl-β-D glucosaminidase (NAG), etc. The main clinical manifestations are oliguric or non-oliguric acute renal insufficiency, accompanied by nausea, vomiting, weight loss, abdominal pain, fatigue, fever, rash and joint pain. Combined renal tubular function damage may manifest as Fanconi syndrome, with the occurrence of glycosuria, aminoaciduria, phosphaturia and proximal renal tubular acidosis; it may also manifest as tubular proteinuria and disorders of water, electrolyte and acid-base balance. Typical drug-related TIN often has a more characteristic course of disease. Renal insufficiency occurs 10 to 20 days after medication. Renal function can slowly recover after medication is stopped. However, when the sensitizing drug is used again, acute renal failure may occur within 2 to 3 days. About 75% of patients have fever symptoms, 30%-50% have transient erythematous rash, itching, maculopapular rash, etc., 30%-60% have peripheral blood eosinophilia, but only about 30% have all three symptoms (triad). Half of the patients have elevated serum IgE levels, and 15%-20% of patients have nonspecific joint pain. Chronic TIN Patients with chronic TIN often lack subjective symptoms and often seek medical treatment due to unexplained increases in serum creatinine, urea nitrogen and uric acid or disorders of electrolytes (especially potassium) and acid-base balance. Some patients may also experience extra-renal symptoms such as weight loss, fatigue, fever, rash, and joint pain, but generally without edema and hypertension. The clinical feature of chronic TIN is severe anemia that is disproportionate to the degree of chronic renal insufficiency. Renal tubular dysfunction is a characteristic change of chronic TIN, clinically manifested as glycosuria, aminoaciduria, small molecule proteinuria, phosphaturia, alkalinuria, hypophosphatemia, hypercalcemia, hyponatremia, hyper- or hypokalemia, and renal tubular acidosis. In addition, nocturia, polyuria, and low specific gravity urine may occur due to the concentration disorder caused by the damage to the renal medulla and renal papilla. |
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